Obesity is a world-wide health problem that is associated with metabolic syndrome, including insulin resistance and the development of type 2 diabetes (Boden, 2003, Exp. Clin. Endocrinol. Diabetes, 111:121-124). Obesity is associated with increased blood levels of free fatty acids (FFA). This increase in FFA is considered to be a causative link between obesity and insulin resistance (Arner, 2002, Diabetes Metab. Res. Rev., 18 Suppl. 2:S5-9; Boden, 2006, Curr. Diab. Rep. 6:177-181; Kahn et al., 2006, Nature, 444:840-846; Kovacs and Stumvoll, 2005, Best Pract. Res. Clin. Endocrinol. Metab., 19:625-635). The mechanism that accounts for FFA-induced insulin resistance is incompletely understood. However, activation of the cJun NH2-terminal kinase (JNK) stress signaling pathway appears to play a major role in the development of obesity-induced insulin resistance (Hirosumi et al., 2002, Nature, 420:333-336). One molecular mechanism that contributes to JNK-induced insulin resistance is the phosphorylation of the insulin receptor adapter protein IRS1 on the inhibitory site Ser-307 (Aguirre et al., 2000, J. Biol. Chem., 275:9047-9054; Aguirre et al., 2002, J. Biol. Chem. 277:1531-1537; Lee et al., 2003, J. Biol. Chem. 278:2896-2902). FFA-stimulated JNK signaling is therefore an important physiological mechanism of insulin resistance.